Childhood Maltreatment and BMI Trajectories to Mid-Adult Life: Follow-Up to Age 50y in a British Birth Cohort.

Childhood maltreatment including abuse and neglect has been associated with adult obesity, but evidence on life-course development of obesity or BMI gain is unclear. We aim to establish whether childhood maltreatments are related to obesity or BMI at different life-stages 7y-50y and to identify possible explanations for associations

Child maltreatment, early life socioeconomic disadvantage and all-cause mortality in mid-adulthood: findings from a prospective British birth cohort

Objectives: Early-life adversities (ELAs) such as child maltreatment (neglect and abuse) and socioeconomic disadvantage have been associated with adult mortality. However, evidence is sparse for specific types of ELA. We aimed to establish whether specific ELAs (ie, different types of child maltreatment and socioeconomic disadvantage) were associated independently with all-cause mortality in mid-adulthood and to examine potential intermediary pathways. / Design: Prospective cohort study. / Setting: 1958 British birth cohort: a longitudinal, population-based sample of individuals born in Great Britain during a single week in March 1958. / Participants: 9310 males and females with data on child maltreatment and mortality (44/45–58 years). / Outcome measures: Mortality follow-up from 2002/2003 to 2016 when participants were aged 44/45–58 years. Death was ascertained via the NHS Central Register (N=296) or cohort maintenance activities (N=16). / Results: Prevalence of ELAs ranged from 1.6% (sexual abuse) to 11% (psychological abuse). Several, but not all, ELAs were associated with increased risk of premature death, independent of covariates and other adversities; adjusted HRs were 2.64 (95% CI 1.52 to 4.59) for sexual abuse, 1.93 (95% CI 1.45 to 2.58) for socioeconomic disadvantage, 1.73 (95% CI 1.11 to 2.71) for physical abuse and 1.43 (95% CI 1.03 to 1.98) for neglect. After adjustment for covariates and other adversities, no associations with mortality were observed for psychological and witnessing abuse. Regarding potential intermediaries (including adult socioeconomic factors, behaviours, adiposity, mental health and cardiometabolic markers), most associations attenuated after accounting for adult health behaviours (particularly smoking). In addition, early-life socioeconomic disadvantage and neglect associations attenuated after accounting for adult socioeconomic factors. The association for sexual abuse and premature mortality was largely unaffected by potential intermediaries. / Conclusions: Associations with premature mortality varied by type of ELA: associations for sexual and physical abuse, neglect and socioeconomic disadvantage were independent of each other. Different types of ELAs could influence premature mortality via different pathways; this requires further research

Obesity and risk factors for cardiovascular disease and type 2 diabetes: Investigating the role of physical activity and sedentary behaviour in mid-life in the 1958 British cohort.

A key public health priority is to minimise obesity-related health consequences. We aim to establish whether physical activity (PA) or less sedentary behaviour ameliorate associations of obesity with biomarkers for cardiovascular disease (CVD) and type 2 diabetes

Combined early and adult life risk factor associations for mid-life obesity in a prospective birth cohort: assessing potential public health impact.

OBJECTIVE: The combined effect of life-course influences on obesity development and thus their potential public health impact is unclear. We evaluated combined associations and predicted probabilities for early and adult life risk factors with central and general obesity in mid-adulthood. SETTING: 1958 British birth cohort. PARTICIPANTS: 4629 males and 4670 females with data on waist circumference. OUTCOME MEASURES: 45 year obesity measured via waist circumference, waist-hip ratio (WHR) and BMI. RESULTS: At 45 years, approximately a third of the population were centrally obese and a quarter were generally obese. Three factors (parental overweight, maternal smoking during pregnancy and adult inactivity) were consistently associated with central and general obesity. Predicted probabilities for waist obesity increased from those with none to all three risk factors (0.15-0.33 in men; 0.19-0.39 in women (ptrend<0.001)), with a similar trend for general obesity. Additional factors (adult smoking, low fibre and heavy alcohol consumption) were associated with WHR obesity, although varying by gender. Prevalence of risk factors was higher in manual than non-manual groups: for example, in men 38% versus 25%, respectively, had ≥2 risk factors for waist and general obesity. CONCLUSIONS: Early-life and adult factors that are amenable to change are highly prevalent and accumulate in association with central and general obesity in mid-adulthood. The increase in probabilities for mid-adult obesity associated with cumulative levels of risk factors suggests the potential for public health impact

Obesity in early adulthood and physical functioning in mid-life: Investigating the mediating role of c-reactive protein

INTRODUCTION: Obesity in adulthood is associated with reduced physical functioning (PF) at older ages. However, mechanisms underpinning this association are not well understood. We investigated whether and the extent to which C-reactive protein (CRP) mediates the association between early-adult obesity and mid-life PF. METHODS: We used data from 8495 participants in the 1958 British birth cohort study. Body mass index (BMI), CRP and PF were measured at 33, 45 and 50y, respectively. Poor PF was defined as the lowest (sex-specific) 10% on the Short-form 36 Physical Functioning subscale. We accounted for prospectively measured confounders in early-life (e.g., social class at birth) and in mid-adulthood (e.g., 42y comorbidities). We decomposed the total effect of early-adult obesity on mid-life PF into direct and indirect (via CRP) effects, by employing a mediation analysis based on parametric g-computation. RESULTS: The estimated total effect of obesity at 33y on poor PF at 50y, expressed as an odds ratio (OR), was 2.41 (95% CI: 1.89, 3.08). The direct effect of obesity on poor PF (i.e., not operating via CRP), was 1.97 (95% CI: 1.51, 2.56), with an indirect effect of 1.23 (95% CI: 1.10, 1.37). As such, the proportion of the total effect which was mediated by the effect of obesity on CRP at 45y, was 23.27% (95% CI: 8.64%, 37.90%). CONCLUSION: Obesity in early-adulthood was associated with over twice the odds of poor PF in mid-life, with approximately 23% of the obesity effect operating via a downstream effect on CRP. As current younger generations are likely to spend greater proportions of their life course in older age and with obesity, both of which are associated with poor PF, there is an urgent need to identify mechanisms, and thus potential modifiable intermediaries, linking obesity to poor PF

Cardiovascular Health and Stroke in Older British Men: Prospective Findings From the British Regional Heart Study.

BACKGROUND AND PURPOSE: Research exploring the utility of cardiovascular health (CVH) and its Life's Simple 7 (LS7) components (body mass index, blood pressure [BP], glucose, cholesterol, physical activity, smoking, and diet) for prevention of stroke in older adults is limited. In the British Regional Heart Study, we explored (1) prospective associations of LS7 metrics and composite CVH scores with, and their impact on, stroke in middle and older age; and (2) if change in CVH was associated with subsequent stroke. METHODS: Men without cardiovascular disease were followed from baseline recruitment (1978-1980), and again from re-examination 20 years later, for stroke over a median period of 20 years and 16 years, respectively. LS7 were measured at each time point except baseline diet. Cox models estimated hazard ratios (95% CI) of stroke for (1) ideal and intermediate versus poor levels of LS7; (2) composite CVH scores; and (3) 4 CVH trajectory groups (low-low, low-high, high-low, high-high) derived by dichotomising CVH scores from each time point across the median value. Population attributable fractions measured impact of LS7. RESULTS: At baseline (n=7274, mean age 50 years), healthier levels of BP, physical activity, and smoking were associated with reduced stroke risk. At 20-year follow-up (n=3798, mean age 69 years) only BP displayed an association. Hazard ratios for intermediate and ideal (versus poor) levels of BP 0.65 (0.52-0.81) and 0.40 (0.24-0.65) at baseline; and 0.84 (0.67-1.05) and 0.57 (0.36-0.90) at 20-year follow-up. With reference to low-low trajectory, the low-high trajectory was associated with 40% reduced risk, hazard ratio 0.60 (0.44-0.83). Associations of CVH scores weakened, and population attributable fractions of LS7 reduced, from middle to old age; population attributable fraction of nonideal BP from 53% to 39%. CONCLUSIONS: Except for BP, CVH is weakly associated with stroke at older ages. Prevention strategies for older adults should prioritize BP control but also enhance focus beyond traditional risk factors

Early adulthood determinants of mid-life leisure-time physical inactivity stability and change: Findings from a prospective birth cohort

OBJECTIVES: Physical inactivity is highly prevalent. Knowledge is needed of influences on inactive lifestyles. We aimed to establish whether early adult factors predict subsequent inactivity patterns in mid-adulthood. DESIGN: Leisure-time inactivity (activity frequency<1/week) was assessed at 33y and 50y in the 1958 British Birth cohort (N=12,271). METHODS: We assessed associations of early adult (23-33y) physical status, mental function, social, family and neighbourhood circumstances with four 33-50y patterns (never inactive, persistently inactive, deteriorating or improving) using multinomial logistic regression with and without adjustment for childhood factors (e.g. social class). RESULTS: Inactivity prevalence was similar at 33y and 50y (∼31%), but 17% deteriorated and 18% improved with age. Factors associated with persistent vs never inactive were: limiting illness (relative risk ratio (RRR):1.21(1.04,1.42) per number of ages exposed (0,1 or 2 times across ages 23y and 33y), obesity (1.33(1.16,1.54) per number of ages exposed), height (0.93(0.89,0.98) per 5cm), depression (1.32(1.19,1.47) per number of ages exposed); education (1.28(1.20,1.38) per decrease on 5-point scale) and neighbourhood (1.59(1.37,1.86) in 'industrial/local authority housing areas' and 1.33(1.12,1.58) in 'growth/metropolitan inner areas' vs 'suburbs, service, rural or seaside areas'). Associations were broadly similar for inactivity deterioration. Industrial/local authority housing areas (0.75(0.61,0.91)) and longer obesity exposure (0.78(0.64,0.95)) were associated with lower RRRs for improvement. Number of children was associated with improvement, although associations varied by age. Associations remained after adjustment for childhood factors. CONCLUSIONS: Several early adult factors are associated with inactivity persistence and deterioration; fewer with improvement. Obesity duration and neighbourhood lived in during young adulthood had long-lasting associations with inactivity patterns in mid-life

Change in health and social factors in mid-adulthood and corresponding changes in leisure-time physical inactivity in a prospective cohort

BACKGROUND: To identify whether changes in adult health and social factors are associated with simultaneous changes in inactivity. METHODS: Health, social factors and leisure-time inactivity (activity frequency < 1/week) were self-reported at 33y and 50y in the 1958 British birth cohort (N = 12,271). Baseline (33y) health and social factors and also patterns of change in factors 33y-to-50y were related to inactivity 33y-to-50y (never inactive, persistently inactive, deteriorating to inactivity, or improving from inactivity) using multinomial logistic regression. RESULTS: Approximately 31% were inactive at 33y and 50y; 35% changed status 33y-to-50y (17% deteriorating to inactivity, 18% improving from inactivity). Baseline poor health and obesity were associated with subsequent (33y-to-50y) inactivity; e.g. for poor health, relative risk ratios (RRRs) for deteriorating to inactivity (vs never inactive) and improving from inactivity (vs persistently inactive) were 1.38(1.16,1.64) and 0.77(0.63,0.94) respectively. Adverse changes in health and weight were associated with simultaneous adverse changes in inactivity; e.g. worsening health (vs always good/excellent health) was associated with higher risk of deteriorating to inactivity (RRR:2.20(1.85,2.62)) and lower risk of improving from inactivity (RRR:0.61(0.49,0.77)). However, improving health and weight loss were not associated with improving from inactivity. Worsening self-efficacy 33y-to-50y was associated with lower risk of improving from inactivity; there was no association between improving self-efficacy and inactivity change. Downward social mobility was not associated with deteriorating to or improving from inactivity. Changes in depression symptom level, marriage/co-habitation or parenthood 33y-to-50y were not associated with inactivity changes. No associations were observed for employment. CONCLUSIONS: Associated changes in mid-life health factors with deleterious inactivity changes, highlight the importance of maintaining health, weight and self-efficacy across adulthood to deter inactivity

Stroke risk in older British men: Comparing performance of stroke-specific and composite-CVD risk prediction tools

Stroke risk is currently estimated as part of the composite risk of cardiovascular disease (CVD). We investigated if composite-CVD risk prediction tools QRISK3 and Pooled Cohort Equations-PCE, derived from middle-aged adults, are as good as stroke-specific Framingham Stroke Risk Profile-FSRP and QStroke for capturing the true risk of stroke in older adults. External validation for 10y stroke outcomes was performed in men (60-79y) of the British Regional Heart Study. Discrimination and calibration were assessed in separate validation samples (FSRP n = 3762, QStroke n = 3376, QRISK3 n = 2669 and PCE n = 3047) with/without adjustment for competing risks. Sensitivity/specificity were examined using observed and clinically recommended thresholds. Performance of FSRP, QStroke and QRISK3 was further compared head-to-head in 2441 men free of a range of CVD, including across age-groups. Observed 10y risk (/1000PY) ranged from 6.8 (hard strokes) to 11 (strokes/transient ischemic attacks). All tools discriminated weakly, C-indices 0.63–0.66. FSRP and QStroke overestimated risk at higher predicted probabilities. QRISK3 and PCE showed reasonable calibration overall with minor mis-estimations across the risk range. Performance worsened on adjusting for competing non-stroke deaths. However, in men without CVD, QRISK3 displayed relatively better calibration for stroke events, even after adjustment for competing deaths, including in oldest men. All tools displayed similar sensitivity (63–73 %) and specificity (52–54 %) using observed risks as cut-offs. When QRISK3 and PCE were evaluated using thresholds for CVD prevention, sensitivity for stroke events was 99 %, with false positive rate 97 % suggesting existing intervention thresholds may need to be re-examined to reflect age-related stroke burden

Childhood maltreatment and biomarkers for cardiometabolic disease in mid-adulthood in a prospective British birth cohort: associations and potential explanations

OBJECTIVES: Research on associations between childhood maltreatment and adult cardiometabolic disease risk is sparse. We aimed to investigate associations between different forms of child maltreatment and mid-adult cardiometabolic markers and whether potential intermediaries could account for the associations observed. SETTING: 1958 British birth cohort. PARTICIPANTS: Approximately 9000 cohort members with data on cardiometabolic markers. OUTCOMES: Adult (45y) cardiometabolic markers (blood pressure, lipids and glycated haemoglobin [HbA1c]). RESULTS: Seventeen per cent of participants were identified as neglected; 6.1%, 1.6% and 10.0% were identified as experiencing physical, sexual and psychological abuse, respectively. Childhood neglect and physical abuse were associated with high body mass index (BMI) and large waist circumference when adjusting for early-life covariates. For neglect, the adjusted odds ratio (AOR) was 1.16 (95% CI: 1.02 to 1.32) and 1.15 (1.02 to 1.30) for general and central obesity, respectively, and for physical abuse, the respective AOR was 1.36 (1.13 to 1.64) and 1.38 (1.16 to 1.65). Neglect was also associated with raised triglycerides by 3.9 (0.3 to 7.5)% and HbA1c by 1.2 (0.4 to 2.0)%, and among females, lower high-density lipoprotein cholesterol (HDL-c) by 0.05 (0.01 to 0.08)mmol/L after adjustment. For physical abuse, the AOR was 1.25 (1.00 to 1.56) for high low-density lipoprotein cholesterol, HbA1c was raised by 2.5 (0.7 to 4.3)% (in males) and HDL-c was lower by 0.06 (0.01 to 0.12)mmol/L (in females). Associations for sexual abuse were similar to those for physical abuse but 95% CIs were wide. For psychological abuse, the AOR for elevated triglycerides was 1.21 (1.02 to 1.44) and HDL-c was lower by 0.04 (0.01 to 0.07)mmol/L. Maltreatments were not associated with raised blood pressure. In analyses of potential intermediary factors, several associations attenuated after adjustment for adult lifestyles (mainly smoking and alcohol consumption rather than physical activity) and child-to-adult BMI. CONCLUSIONS: Childhood maltreatments, particularly neglect and physical abuse, were associated with greater adiposity and poorer lipid and HbA1c profiles decades later in adulthood. Associations were modest but independent of early-life factors linked to these outcomes. Findings implicate adult lifestyles as an important intermediary between child maltreatment and outcomes